Ben writes:
To Innocent Varicella and Cell Needs (yay for biology anagrams)
After listening to the entire TWiP and TWiM catalogues, I am onto TWiEVO and loving it. Evolutionary biology requires such a different way of thinking than the molecular biology I’m used to, but that kind of thinking can be incredibly important when considering key questions of molecular biology.
While listening to some of the episodes about the evolution of sexual reproduction I began questioning some of the evolutionary drivers where sexual reproduction is favoured. This is well outside my normal field, so my understanding here may be flawed, but I’ve heard that in many instances sexual reproduction is speculated to have evolved as a strategy to prevent mass extinction or significant reductions in fitness by pathogens/parasites. Considering this, it’s logical then to speculate that parasites such as the Plasmodium spp. parasites that cause malaria, could have evolved sexual replication strategies to avoid immune clearance.
My question then is, if sexual replication could evolve (in many separate instances) as a mechanism for avoiding pathogenic insults or avoiding immune clearance, what barriers prevent this from occurring in pathogenic bacteria or bacteria/archaea that are infected by lytic phage? Conjugation has clear parallels to sexual replication but is not linked to replication and is therefore fundamentally different, which raises the reciprocal question of what might have prevented conjugation from evolving as a diversification strategy amongst protozoans and multicellular organisms?
Would love to hear what you think about these very spicy questions!
May TWiEVO remain under positive selection,
Regards,
Ben
—
Ben Liffner
PhD Candidate – Malaria Biology Lab (Wilson Lab)
Research Centre for Infectious Diseases
School of Biological Sciences
The University of Adelaide
Anthony writes:
Re Giant viruses #49
Where the large number of genes came from is important. Why they are still there is too. There must be a cost with the production of a large genome — including time. Even though the resources come from a host, using them up means less virus at the end. Might the giant viruses have come from ancient phages whose bacteria hosts were the prey of amoeba and other unicellular eukaryotes? It would be a neat trick to simply abandon ship on the consumed bacteria and then to infect the predator.
It seems to me that the size of the giants is what allows them to forego receptors and just wait for phagocytosis. The question then is why did the intermediate steps happen? What advantage would there be for a virus to be a little bigger, but still too small for an amoeba to bother with? I’m speculating of an intermediate of being eaten while inside the original bacteria host. Extra genes would then be useful so that the amoeba could be reprogrammed to emulate however necessary for virus replication the original bacteria host’s functionality.
For the viruses found in permafrost, they were happy in a lab with current amoeba. It would seem unlikely that amoeba from far away in place and time would work so well. Perhaps they did because the giant virus has something of a Swiss Army Knife in its genome.
FWIW
Michael writes:
Dear Vincent, Nels, Rich, and the rest of the TwiV team,
As a fourth year grad student at Michigan State University (Plant Bio), I often find myself enjoying TWiX podcasts as I commute to East Lansing and to my various research sites around the state.
Recently, I had the pleasure of listening to the following three podcasts in a single week:
The first: TWiEvo 48 (“Flipping out with choanos on caffeine…)
The second: TWiV 575 (“Endless giant virus forms most beautiful”)
The third: TWiEvo 49 (“A giant podcast on giant viruses”).
Listening to these three podcasts (in that particular order), was the most intellectually satisfying podcast consumption I’ve ever had!
All three episodes represent solid individual units, but, as a trio, they build on one another conceptually and thematically—culminating in TWiEvo 49 with an exciting conversation in which Vincent, Nels, and Rich review the giant virus conference while making connections to material introduced in the other two episodes.
I’m a plant biologist and an ecologist by training, but I’m focusing my dissertation research on exploring the ecology and evolution of ‘wild’ (i.e., non-crop) plant-virus interactions. The stuff you guys talked about in this trio of episodes—viruses as gene thieves, virus proteins involved in host enzymatic pathways, virus genes being incorporated into host genomes—this is the stuff that keeps me up at night! As we continue to learn more about the diversity and abundance of viruses that inhabit all the nooks and crannies of our great planet, I am hoping that community ecologists take note—viruses can influence processes that shape communities and mediate biodiversity!
Needless to say, I was thrilled to hear that Vincent is incorporating an ecological unit into his virology course. Based on the recent marine-themed TWiVs, I’m sure you’ll have plenty of marine ecology included in the unit, but don’t forget about terrestrial ecosystems! You’re already familiar with the Marquez et al (2007) paper (three-way symbiosis that confers heat tolerance to a plant), but I want to point you to a series of papers that highlight the role of a plant virus in facilitating a dramatic shift in the community composition of California grasslands (spoiler: exotic annual grasses invade and takeover native grasslands by way of Barley yellow dwarf virus) (Malmstrom et al 2005a, 2005b; Borer et al 2007) (links to papers provided below).
The lead author on the 2005 papers (Carolyn Malmstrom) is my adviser, and the person responsible for my new-found obsession with viruses. As a recent newcomer to the field of virology, your podcasts have been a wonderful resource for me as I try to wrap my head around how viruses work (and they were particularly helpful for me in preparing for my comprehensive exams a while back!).
Thanks to all of you for your contributions to these podcasts—they are important!
Kind regards,
Mike Ryskamp
PhD Candidate
Plant Biology Program
Michigan State University
East Lansing MI
Links to papers:
Marquez et al (2007) https://science.sciencemag.org/content/315/5811/513/tab-pdf
Malmstrom et al (2005a):
https://link.springer.com/article/10.1007/s00442-005-0099-z
Malmstrom et al (2005b):
https://nph.onlinelibrary.wiley.com/doi/full/10.1111/j.1469-8137.2005.01479.x
Borer et al (2007):